Mink homozygous for the Aleutian gene (aa) and standard dark mink (A-) were injected with high doses of tissue culture (Utah-1) or mink passaged (Pullman-1) Aleutian Mink disease (AMD) virus. Aleutian mink developed specific antibody 7 to 10 days post inoculation (PI) when injected with the Utah-1 strain or 10 to 14 days PI when injected with the Pullman strain. Irrespective of genotype or virus strain, all animals injected developed marked hypergammaglobulinemia (HGA) within 8 to 10 weeks which persisted over an extended period of time (24 weeks). Blood Urea Nitrogen (BUN) was measured to monitor kidney damage during the progression of the disease. Mink, particularly of the aa genotype which developed BUN levels of 180 to 200 mg percent and clinical signs of uremia (ulcers and bleeding) became moribund and had to be sacrificed. Using affinity chromatography with immobilized equine CIq, immune complexes were isolated from infected mink sera which had developed an antibody response. The levels of circulating immune complexes (IC) increased with progression of the HGA. As purified IC were infectious for mink and had high antibody activity as demonstrated by Counter current immunoelectrophoresis, we believe that a large portion of the immune aggregates consisted of infectious AMD virus antibody complexes, which is consistent with the assumption of AMD being an IC mediated disease. BIBLIOGRAPHIC REFERENCE: Svehag, SE and D. Burger 1976: Isolation of CIq binding immune complexes by affinity chromatography and desorption with a diamino-alkyl compound. Acta Pathol. and Microbiol. Scandinavica 84C:116.